The two-spotted spider mite Tetranychus urticae is a cosmopolitan agricultural pest with an extensive host plant range. The species shows clear photoperiodism. Adult females reproduce under long days, whereas they enter reproductive diapause in response to short days. Diapausing females terminate diapause and start oviposition under long days, whereas they maintain diapause under short days. Physiological mechanisms underlying photoperiodism are considered to be divided into 4 processes (photoreceptor, photoperiodic time measurement, counter, endocrine system), and now we accumulate much information on each of the processes in this species. In this review, we introduce recent advances in our knowledge on physiological and genetic mechanisms governing photoperiodism of T. urticae.

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Emerging data suggest an important relationship between sleep and Alzheimer’s disease (AD), but how poor sleep promotes the development of AD remains unclear. Using a Drosophila model of AD, we provide evidence suggesting that changes in neuronal excitability underlie the effects of sleep loss on AD pathogenesis.β-amyloid (Aβ) accumulation leads to reduced and fragmented sleep, while chronic sleep deprivation increases Aβ burden. Moreover, enhancing sleep reduces Aβ deposition. Increasing neuronal excitability phenocopies the effects of reducing sleep on Aβ, and decreasing neuronal activity blocks the elevated Aβ accumulation induced by sleep deprivation. At the single neuron level, we find that chronic sleep deprivation, as well as Aβ expression, enhances intrinsic neuronal excitability. Importantly, these data reveal that sleep loss exacerbates Aβ-induced hyperexcitability and suggest that defects in specific K(+) currents underlie the hyperexcitability caused by sleep loss and Aβ expression. Finally, we show that feeding levetiracetam, an anti-epileptic medication, to Aβ-expressing flies suppresses neuronal excitability and significantly prolongs their lifespan. These findings directly link sleep loss to changes in neuronal excitability and Aβ accumulation and further suggest that neuronal hyperexcitability is an important mediator of Aβ toxicity. Taken together, these data provide a mechanistic framework for a positive feedback loop, whereby sleep loss and neuronal excitation accelerate the accumulation of Aβ, a key pathogenic step in the development of AD.

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In foraging situation, starving animals that possess sophisticated appendages exhibit dexterous manipulative behavior whose goal is to accomplish feeding. We aimed to understand neurophysiological mechanisms underlying goal-directed manipulative behavior that is based on their internal motivation for satiation, and hence adopted American lobster Homarus americanus as an experimental animal. The lobster has a pair of asymmetrical claws as the first thoracic appendages, one of which is developed as crusher claw. The crusher is utilized for gripping clamshell in their ecological foraging context. We developed reward operant conditioning systems for training the animals to grip a bar for food, and demonstrated that the frequency of gripping behavior can be controlled by the learning system in both free-moving and semi-restrained conditions. We also showed that the behavior can be induced by light stimuli as discriminative cues. Finally, we quantitatively characterized goal-directed gripping behavior in the lobster at the level of motor output by applying chronic electromyographic analysis. The series of our studies would be regarded as pioneering works for purveying a basis of neurophysiological investigation of goal-directed manipulative behavior in micro-brain animals.

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